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APEX > Unit 12 - Misc. Topics > Flashcards

Unit 12 - Misc. Topics Flashcards

1
Q

most effective single method of perioperative warming

A

forced air warmer

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2
Q

afferent limb of temperature regulation

A

thermoreceptors
- skin
- deep tissue
- spinal cord

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3
Q

control center of temperature regulation

A
  • hypothalamus (preoptic region)
  • brainstem
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4
Q

efferent responses to hypothermia

A
  • vasoconstriction
  • piloerection
  • shivering
  • nonshivering thermogenesis
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5
Q

efferent response to hyperthermia

A
  • vasodilation
  • diaphoresis
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6
Q

4 mechanisms of heat transfer

A
  1. radiation
  2. convection
  3. evaporation
  4. conduction
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7
Q

how does a patient lose heat via infrared radiation

A

if the patient is warmer than the environment, then heat is lost to the environment

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8
Q

what type of heat transfer does covering the patient reduce

A

radiant

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9
Q

number 2 source of heat loss

A

convection

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10
Q

what is convection?
what % of periop heat transfer does it account for?

A

transfer of heat by movement of matter

15-30%

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11
Q

how is heat lost via convection?

A

air movement over the body whisks away heat that has radiated from the body

the body radiates more heat to replace what was taken away by airflow

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12
Q

how does laminar flow affect the amount of heat lost to convection

A

increases

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13
Q

amount of energy to vaporize water

A

latent heat of vaporization

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14
Q

what % of heat transfer does evaporation account for in the periop pt

A

20%

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15
Q

how can water be lost by evaporation during surgey?

A
  • respirations
  • wounds
  • internal organ exposure
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16
Q

the rate of this process is a function of the exposed surface area and the relative humidity of the environment

A

evaporation

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17
Q

what is conduction?

what % of heat transfer does this account for in periop pt?

A

heat is lost when the patient comes into direct contact with a cooler object

< 5%

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18
Q

examples of heat loss through conduction

A
  • cold OR table
  • cold IV fluids
  • cold irrigation fluids
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19
Q

the amount of conductive heat loss is a function of:

A

the temperature gradient and thermal conductivity of the object

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20
Q

phase 1 of intraoperative heat transfer

how long does this phace last?

A

heat redistribution from core to periphery

first hour after induction of anesthesia

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21
Q

what is phase 2 of intraoperative heat transfer?

when does this occur?

A

heat transfer is greater than heat production

hours 1-5 after induction

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22
Q

what is phase 3 of intraoperative heat transfer?

when does this occur?

A

equilibrium develops between heat lost to environment and heat production

hours 5-7 after induction

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23
Q

what causes heat redistribution during general, spinal, or epidural anesthesia?

A

redistribution of heat from central compartment to peripheral compartment

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24
Q

perioperative events contributing to heat loss

A
  • recalibration of the hypothalamic set point
  • drug induced vasodilation
  • impaired shivering
  • core to peripheral temperature redistribution
  • cool ambient temp
  • cold OR table
  • admin of room temp fluids and cold blood products
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25
Q

what is the most significant source of heat loss in the OR?

A

radiation

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26
Q

what is the least significant source of heat loss in the OR?

A

conduction

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27
Q

a heat lamp is an example of what type of heat transfer

A

radiation

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28
Q

what temp monitoring site offers the best combination of accuracy and safety over an extended period of time

A

esophageal

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29
Q

CV consequences of periop hypothermia

A
  • SNS stimulation
  • vasoconstriction, decreased tissue PaO2
  • coagulopathy, plt dysfunction
  • hgb S sickling
  • oxyhgb dissociation curve shifts to the left
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30
Q

how does hypothermia affect the oxyhgb dissociation curve

A

shifts to the left

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31
Q

pharmacologic consequences of hypothermia

A
  • slowed drug metabolism
  • increased solubility of volatiles
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32
Q

how does shivering increase the risk of myocardial ischemia and infarction

A

increases O2 consumption by 400-500%

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33
Q

pharmacologic modalities used to treat postop shivering

A
  • meperidine
  • clonidine
  • dexmedetomidine
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34
Q

how does hypothermia affect O2 consumption?

A

reduces by 5-7% for every 1 degree C reduction in body temp

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35
Q

when might induced hypothermia be useful?

A
  • cerebral ischemia (stroke)
  • cerebral aneurysm clipping
  • TBI
  • bypass
  • cardiac arrest
  • aortic cross clamping
  • CEA
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36
Q

what type of temperature monitoring site reflects temp of vital organs?

A

core body temp

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37
Q

ideal position of esophageal temp probe

A

distal 1/3 to 1/4th of esophagus

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38
Q

placement of adult esophageal temp probe

A

38-42cm past incisors

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39
Q

placement of esophageal temp probe in an adult with a 2nd generation SGA

A

15-20 cm distal to drain tube

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40
Q

pediatric placement of esophageal temp probe

A

10 + (2x age in yrs) / 3 cm past incisors

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41
Q

why is esophageal temp increased if placed in stomach

A

due to heat created by liver metabolism

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42
Q

why may temp be decreased if esophageal temp probe is placed in proximal esophagus

A
  • cool inspiratory gas
  • continuous gastric suction
  • thoracotomy
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43
Q

ideal position of nasopharyngeal temp prob and why

A

sensor contacts posterior nasopharyngeal wall posterior to soft palate

close to hypothalamus

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44
Q

what causes decreased temp reading of nasopharyngeal temp probe

A

leakage of inspiratory gas

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45
Q

ideal position of rectal temp probe

A

8 cm in adults, 3 cm in children

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46
Q

what causes temp reading of rectal temp probe to be increased or decreased

A
  • increased: heat producing bacteria in the gut
  • decreaesd: cool blood from lower extremities, stool
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47
Q

temperature measurement sites that lag during rapid warming and cooling

A
  • rectal
  • bladder
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48
Q

what causes bladder temp to read low?

A

inadequate UOP

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49
Q

when is temp reading via pulmonary artery not reliable?

A
  • CBP
  • thoracotomy
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50
Q

skin temp is often ___ deg C less than core temp

A

2-4

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51
Q

how can skin temp be used to assess onset of a regional block?

A

temp will rise if the block is good d/t sympathectomy-induced rise in peripheral blood flow

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52
Q

5 clinically relevant CV consequences of perioperative hypothermia

A
  1. myocardial ischemia/arrythmias
  2. decreased DO2
  3. surgical site infection
  4. increased blood loss (coagulopathy)
  5. risk of sickle cell crisis in pts with SCD
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53
Q

why should saline be added to the ETT cuff vs. air for removal of vocal cord papilloma with laser

A
  1. acts as a heat sink for thermal energy produced by the laser
  2. if laser breaks the balloon, surgeon will see saline in surgical field (more obvious if dyed)
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54
Q

eye protection needed when CO2 laser is used

A

clear lenses

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55
Q

3 ingredients to produce a fire

(components of fire triangle)

A
  1. ignition source (cautery, laser)
  2. fuel (ETT, drapes, surgical supplies)
  3. oxidizer (O2, N2O)
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56
Q

5 steps to take when fire is present in the OR

A
  1. stop ventilation, remove ETT
  2. stop flow of all airway gases
  3. remove other flammable material from airway
  4. pour water or saline into airway
  5. if fire isn’t extinguished on 1st attempt, use a CO2 fire extinguisher
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57
Q

3 steps to take after OR fire is controlled

A
  1. re-establish ventilation via mask. avoid supplemental O2 or N2O
  2. check ETT for damage - fragments may be in pt’s airway
  3. perform bronch to inspect for retained fragments
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58
Q

what is LASER an acronym for

A

Light Amplification by Stimulated Emission of Radiation

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59
Q

3 things that make laser light different from ordinary light

A

it is
1. monochromatic (light is a single wavelength)
2. coherent (light oscillates in same phase)
3. collimated (light exists as a narrow parallel beam)

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60
Q

which absorbs more water - long wavelength lasers or short?

A

long

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61
Q

which lasers penetrate deeper into tissue - long or short wavelength?

A

short

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62
Q

wavelength of CO2 lasers

A

10,600 nm

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63
Q

type of laser used in oropharyngeal and vocal cord surgeries

A

CO2

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64
Q

structure damaged by CO2 lasers

A

cornea

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65
Q

wavelength of Nd:YAG lasers

A

1064 nm

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66
Q

type of lasers used for tumor debulking and tracheal surgeries

A

Nd:YAG

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67
Q

structure damaged by Nd:YAG lasers

A

retina

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68
Q

eye protection for Nd:YAG lasers

A

green goggles

(Nd:YAG=Green)

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69
Q

wavelength of ruby lasers

A

694 nm

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70
Q

type of laser used for retinal surgery

A

ruby

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71
Q

structure damaged by ruby laser

A

retina

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72
Q

eye protection for ruby lasers

A

red goggles

(Ruby = Red)

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73
Q

wavelength of argon lasers

A

515 nm

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74
Q

type of surgery argon lasers are used for

A

vascular lesions

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75
Q

structure damaged by argon laser

A

retina

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76
Q

eye protection for Argon lasers

A

Amber goggles

(Argon = Amber)

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77
Q

which component of the ETT is the most vulnerable to lasers

A

cuff

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78
Q

T/F - laser resistant tubes have laser resistant cuffs

A

false

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79
Q

why do laser resistant ETTs have 2 cuffs

A

the proximal cuff is filled with saline/dye. if it is perforated by laser, the distal cuff will hopefully remain intact and permit continued PPV

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80
Q

what should determine the choice of ETT in laser surgeries

A

type of laser and its wavelength

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81
Q

which ETT is a good choice for CO2 laser use

A

LaserFlex

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82
Q

which ETT is a good choice for Nd:YAG laser

A

Lasertubus

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83
Q

techniques that do not require an ETT (removing 1 component of fire triangle)

A
  • spontaneous ventilation
  • intermittent PPV via facemask and apnea
  • jet ventilation
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84
Q

why is gas embolus a risk of laser surgery?

A

gas may be used to cool the tip of the laser probe

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85
Q

T/F - laser resistant ETTs reduce the risk of fire when ESU cautery is used

A

false

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86
Q

how to protect pt’s eyes in laser surgery

A
  • tape eyes closed
  • avoid petroleum-based lubricants
  • cover eyelids with saline-soaked gauze
  • use protective glasses
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87
Q

best ways to protect yourself against laser plume

A
  • smoke evacuator
  • high-efficiency masks
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88
Q

what creates a plume of fine particulates with lasers?

A

tissue vaporization

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89
Q

rule of nines (adult)

A

head = 10%
trunk = 36%
arm = 9%
leg = 18%
perineum = 1%

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90
Q

involvement of a 1st degree burn

A

epidermis only

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91
Q

involvement of a 2nd degree burn

A

superficial: epidermis to upper dermis
deep: epidermis to lower dermis

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92
Q

involvement of 3rd degree burn (full thickness burn)

A

subcutaneous tissue
complete destruction of epidermis and dermis

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93
Q

involvement of a 4th degree (full thickness) burn

A

extends to muscle and bone

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94
Q

what burn stages have no sensation d/t obliterated nerve endings

A

3rd & 4th degree

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95
Q

rule of nines (child)

A

head = 19% (9.5% per front/back)
trunk = 16% (each side)
leg = 15%
arm = 9.5%
palm (excluding fingers) = 1%

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96
Q

general rule for rule of nines and head surface area in children

A

for every year > 1 year up to 10 years, you can decrease the head surface area by 1% and increase each leg by 0.5%

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97
Q

best IV fluid to give in initial 24 hours after major burn

A

LR

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98
Q

why should albumin be avoided in the first 24 hours after a major burn?

A

lost to interstitial space

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99
Q

what creates a capillary leak immediately after a burn?

A

increased microvascular permeability

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100
Q

what consequences of capillary leak after burn injury result in edema formation

A
  • increased vascular permeability
  • loss of protein-rich fluid to interstitial space, decreased plasma oncotic pressure
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101
Q

what are fluid requirements in the first 24 hours following a burn?

A

fluid shifts and edema formation are the greatest in the first 12 hours and begin to stabilize by 24 hours

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102
Q

what lab value sugests inadequate volume resuscitation in the first few days of a burn

A

rising hgb

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103
Q

when to consider transfusion in burn pt

A

Hct < 20 (healthy pt)
Hct < 30 (pre-existing CV disease)

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104
Q

Parkland formula

A

first 24 hours:
- 4 mL LR x % TBSA burned x kg
- give 1/2 in first 8 hours
- 1/2 in next 16 hours

second 24 hours:
- D5W mainenance rate
- 0.5 mL colloid x % TBSA x kg

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105
Q

Modified Brooke Formula

A

first 24 hours:
- 2 mL LR x % TBSA x kg
- 1/2 in first 8 hours
- 1/2 in next 16 hours

second 24 hours:
- D5W MIVF
- 0.5 mL colloid x % TBSA burned x kg

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106
Q

clinical end points of burn resuscitation - UOP

A

adult: > 0.5 mL/kg/hr
child (<30 kg): > 1 mL/kg/hr
high voltage electrical injury: > 1-1.5 mL/kg/hr (myoglobin is nephrotoxic)

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107
Q

clinical end points of burn resuscitation: blood pressure

A

adult: MAP > 60
infant: SBP > 60
child: SBP 70-90 + (2 x age in yrs)

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108
Q

clinical end points of burn resuscitation: base deficit

A

< 2

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109
Q

clinical end points of burn resuscitation: oxygen delivery index

A

600 mL O2/min/m2

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110
Q

clinical end point of burn resuscitation: mixed venous oxygen tension (PvO2)

A

35-45 mmHg

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111
Q

why is it important to maintain a higher UOP with electrical burns

A

myoglobinemia is caused by extensive muscle damage - myoglobin is nephrotoxic

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112
Q

what defines abdominal compartment syndrome

A

IAP > 20 mmHg + evidence of organ dysfunction (HD instability, oliguria, increased PIP)

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113
Q

treatment of abd compartment syndrome

A
  • neuromuscular blockade
  • sedation
  • diruesis
  • abdominal decompression vs. laparotomy
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114
Q

CO binds to hgb with an affinity of ____x that of O2

A

200

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115
Q

how does carbon monoxide
affect the oxyhgb dissociation curve

A

shifts to the left, impairs offloading of O2 to tissues
(left = love)

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116
Q

acid-base abnormality seen in CO poisoning

A

metabolic acidosis (inadequate O2 delivery and utilization)

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117
Q

why is the pulse ox not accurate in CO poisoning?

A

it’s unable to distinguish between HgbO2 and HgbCO
may be falsely elevated

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118
Q

treatment of CO poisoning

A

100% O2
hyperbaric oxygen

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119
Q

first priority in treatment of all burn pts

A

high FiO2

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120
Q

gold standard for diagnosing extent of airway inujry in burns

A

fiberoptic bronch

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121
Q

why should a surgical airway only be used as a last resort in burn pts

A

increases risk of pulmonary sepsis and late pulmonary complicaitons

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122
Q

when does upregulation of extrajunctional receptors begin in burn pts

what is the significance of this?

A

after 24 hours

succs is safe within first 24 hours after burn - use after 24 hours can cause lethal hyperkalemia

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123
Q

dosing nondepolarizing NMBs in burn pts

A

increase 2-3 fold (more receptors)

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124
Q

mechanisms of heat loss in a burn pt

A
  • 60% radiation
  • 25% evaporation
  • 12% convection
  • 3% conduction

*normal heat loss: radiation 60%, convection 15-20%, evaporation 20%, conduction < 5%

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125
Q

metabolic changes in burn pts

A

hypermetabolic
- increased catabolism
- increased O2 consumption
- increased HR
- increased RR

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126
Q

ANS activity during ECT

A

initial response: increased PNS activity during tonic phase (~15 seconds)
secondary response: increased SNS activity during clonic phase (lasts several minutes)

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127
Q

how does LIthium affect NMBs

A

prolongs succs and NDNMBs

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128
Q

neuro effects of the clonic phase of ECT-induced seizures

A
  • increased ICP
  • increased CBF
  • increased IOP
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129
Q

absolute contraindications to ECT

A
  • recent MI ( <4-6 months)
  • recent intracranial surgery ( <3 months)
  • recent stroke (<3 months)
  • brain tumor
  • unstable c spine
  • pheochromocytoma
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130
Q

relative contraindications to ECT

A
  • pregnancy
  • pacemaker/ICD
  • CHF
  • glaucoma
  • retinal detachment
  • severe pulmonary disease
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131
Q

minimum recommended seizure duration for ECT

A

25 seconds

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132
Q

drugs that increase seizure duration

A
  • etomidate
  • ketamine
  • alfentanil with propofol
  • aminophylline
  • caffeine
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133
Q

drugs that decrease seizure duration

A
  • propofol
  • versed
  • ativan
  • fentanyl
  • lidocaine
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134
Q

gold standard anesthetic for ECTs. why?

A

methohexital - rapid recovery, no effect on sz duration

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135
Q

negative side effects of etomidate for ECTs

A
  • myoclonus
  • increased PONV
  • more HTN
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136
Q

negative effects of ketamine for ECT

A
  • increased SNS response
  • prolonged recovery
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137
Q

why is glycopyrrolate used for ECTs

A
  • antisialagogue
  • reduced bradycardia/asystole
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138
Q

use of esmolol in ECTs

A

blunts SNS response

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139
Q

how do hyper and hypoventilation impact seizure duration with ECT

A

hypo: decreased
hyper: increased

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140
Q

interaction between MAOIs and indirect acting sympathomimetics

A

HTN crisis

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141
Q

are oral and gastric secretions increased during the initial or secondary response to ECT

A

initial

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142
Q

how does lidocaine affect sz duration in ECTs

A

decreased sz activity

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143
Q

does esmolol affect sz activity in ECTs?

A

nope

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144
Q

how does clonidine affect sz activity in ECTs

A

doesn’t

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145
Q

cause of neuroleptic malignant syndrome

what is the antidote?

A

dopamine depletion in basal ganglia and hypothalamus

bromocriptine (restores dopamine concentrations in these regions)

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146
Q

cause of serotonin syndrome

what is the antidote

A

excess 5-HT activity in CNS and PNS
cyproheptadine (5-HT antagonist)

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147
Q

antitode for anticholinergic poisoning

A

physosigmine (only cholinesterase inhibitor that lacks quarternay ammonium and diffuses into CNS to increase ACh concentration)

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148
Q

key features of malignant hyperthermia

A
  • hypercarbia
  • tachycardia
  • myoglobinemia
  • acidosis
  • muscle rigidity
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149
Q

symptoms that NMS and MH have in common

A
  • muscle rigidity
  • hyperthermia
  • tachycardia
  • acidosis
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150
Q

drug used to treat both NMS and MH

A

dantrolene

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151
Q

what drugs increase risk of serotonin syndrome when combined with SSRIs

A

fentanyl, meperidine

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152
Q

what drugs increase risk of serotonin syndrome when combined with MAOIs

A

meperidine, ephedrine

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153
Q

what drugs increase risk of serotonin syndrome when combined with methylene blue

A

other serotonergic drugs

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154
Q

intraocular perfusion pressure =

A

MAP - IOP

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155
Q

how long is N2O contraindicated for after an intraocular SF6 bubble is placed

A

10 days after

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156
Q

main blood supply to the eye
where does it branch off?

A

opthalmic artery
branches off internal carotid near circle of Willis

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157
Q

what transports venous blood to the cavernous sinus?

A

superior and inferior opthalamic veins

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158
Q

what is the main blood supply to the eye

A

opthalamic artery

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159
Q

what 3 components determine IOP

A
  • chorodial blood volume
  • aqueous fluid volume
  • extraocular muscle tone
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160
Q

what is normal IOP

A

10-20 mmHg

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161
Q

what produces aqueous humor?

where is aqueous humor reabsorbed?

A

produced by ciliary process

reabsorbed by Canal of Schlemm

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162
Q

intraoperative events that increase IOP

A
  • hypercarbia
  • hypoxemia
  • increased CVP
  • increased MAP
  • DL
  • straining/coughing
  • succinylcholine
  • N2O (if SF6 bubble in place)
  • Trendelenberg
  • Prone
  • external compression by facemask
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163
Q

intraoperative events that decrease IOP

A
  • hypocarbia
  • decreased CVP
  • decreased MAP
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164
Q

anesthetic agents that decrease IOP

A
  • volatiles
  • N2O
  • NDNMBs
  • propofol
  • opioids
  • benzos
  • hypothermia
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165
Q

do anticholinergics increase IOP

A

nope

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166
Q

how does LMA placement vs DL effect IOP

A

LMA: minimal
DL: increased

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167
Q

how does succinylcholine affect IOP

A

increases by 5-10 mmHg for up to 10 min
*not reliably blocked by defasciculating NMB

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168
Q

what NMB should be used in an open globe injury

A

full stomach/difficult airway - succs
otherwise - roc

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169
Q

dose of rocuronium for an open globe injury

A

1.2 mg/kg (RSI dose)

170
Q

drugs that decrease aqueous humor production

A
  • acetazolamide (inhibits carbonic anhydrase)
  • timolol (nonselective beta agonist)
171
Q

2 ways drugs can decrease IOP

A
  • decrease aqueous humor production
  • facilitate aqueous humor drainage
172
Q

drug that facilitates aqeous humor drainage

anesthetic implications of this drug

A

echothiophate (irreversible cholinesterase inhibitor)

can prolong duration of succs and ester type LAs

173
Q

2 key considerations for strabismus surgery

A
  1. incrased risk PONV
  2. increased risk of activating oculocardiac reflex
174
Q

nerves that make up oculocardiac reflex

A

CN V (afferent)
CN X (efferent)

175
Q

N2O considerations for eye surgery

A

if a sulfur hexafluoride bubble (SF6) is placed, N2O can expand the bubble and cause blindness

d/c 15 min before bubble placed

avoid for 7-10 days after bubble placed

176
Q

SF6 alternatives and times to avoid N2O

A

silicone oil = 0 days
air bubble = 5 days
perfluopropane (C3F8) = 30 days

177
Q

what causes open angle glaucoma

A

sclerosis of trabecular meshwork; impairs aqueous humor drainage

178
Q

procedures TAP block is best suited for

A

abdominal procedures involving T9-L1 distribution (general, GYN, urologic)

179
Q

abdominal wall structures from superficial to deep

A
  • sub q tissue
  • external oblique
  • internal oblique
  • transverse abdominis
  • peritoneum
180
Q

where does innervation of the anterolateral abdominal wall arise from?

how are these nerves blocked?

A

T7-L1

blocked by placing LA below fascial plane between IO and TA

181
Q

where is US placed for TAP block

A

a few cm superior and parallel to iliac crest

182
Q

2 pops felt during blind technique for TAP block

A
  1. after needle transverses EO
  2. after needle transverses IO
183
Q

volume of LA injected for TAP block

A

15-20 mL per side

184
Q

complications of TAP block

A
  • peritoneal puncture
  • liver hematoma
185
Q

what is a TAP block?

A

unilateral peripheral nerve block that targets nerves of anterior and lateral abdominal wall

186
Q

what 3 landmarks form the triangle of Petit?

A
  1. EO
  2. latissimus dorsi
  3. iliac crest
187
Q

where should LA be injected when placing a TAP block?

A

in fascial plane between IO and TA muscles

188
Q

algogenic

A

stimulus that is expected to produce pain

189
Q

pain due to a stimulus that doesn’t normally produce pain is called:

190
Q

exaggerated pain response to a painful stimulus is called:

A

hyperalgesia

191
Q

pain localized to a dermatome is called:

192
Q

(ex. burning sensation from diabetic neuropathy) is called:

A

dysesthesia

193
Q

paresthesia

A

abnormal sensation described as pins and needles

194
Q

inhibitory neurotransmitters used by the descending inhibitory pain pathway

A

norepinephrine
serotonin

195
Q

antidepressants that can be used to treat chronic pain

A

TCAs
SSRIs
SNRIs

196
Q

CV side effects of TCAs

A
  • prolonged QT
  • orthostatic hypotension
197
Q

what characterizes complex regional pain syndrome

A

neuropathic pain with autonomic involvement

198
Q

risk factors for complex regional pain syndrome

A
  • female
  • previous trauma
  • previous surgery
199
Q

key distinction between type 1 and type 2 complex regional pain syndrome

A

type 2 always preceded by nerve injury; type 1 is not

200
Q

treatments for complex regional pain syndrome

A
  • ketamine
  • memantine (NMDA antagonist)
  • gabapentin
  • regional sympathetic blockade
  • PT
  • steroids
  • amitriptyline
201
Q

what is a thoracic paravertebral block

A

LA injected into paravertebral space to target ventral ramus of spinal nerve as it exits vertebral foramen

202
Q

what does a thoracic paravertebral block cover

A

unilateral sensory and sympathetic block along that specific dermatome

203
Q

how many dermatomes are covered by a thoracic paravertebral block?

A

one - the level injected

204
Q

what types of surgeries see pain relief with a thoracic paravertebral block

A
  • breast
  • thoracotomy
  • rib fracture
205
Q

block useful for cancer pain of upper abdominal organs

A

celiac plexus block

206
Q

complications of a celiac plexus block

A
  • orthostatic hypotension
  • retroperitoneal hematoma
  • hematuria
  • diarrhea
  • AAA dissection
  • back pain
  • retrograde migration of injectate
207
Q

nerve block useful in management of cancer pain of pelvic organs

A

superior hypogastric plexus block

208
Q

complications of hypogastric plexus block

A

retrograde migration of injectate

209
Q

use of a sphenopalatine block

A

relieve postdural puncture headache

210
Q

only cranial nerve that is part of the CNS

A

optic nerve

211
Q

complication of retrobulbar block causing blindness (contralateral amaurosis)

A

LA injected into optic sheath (can migrate toward optic chiasm and anesthetize CN II & III on the side opposite the block)

212
Q

what is post-retrobulbar block apnea syndrome

when is it usually evident?

A

LA that reaches the brainstem and causes apnea

2-5 min after injection

213
Q

when does spontaneous ventilation normally return after post-retrobulbar block apnea syndrome

A

in 15-20 minutes

214
Q

when should you anticipate development of post-retrobulbar block syndrome?

A

assess contralateral pupil - if pupil starts small but dilates shortly after the block, anticipate apnea syndrome

215
Q

risks assoc. with aminoglycosides

examples of aminoglycosides

A
  • ototoxicity, nephrotoxicity, skeletal muscle weakness
  • gentamycin, streptomycin
216
Q

adverse effects of tetracyclines

A
  • hepatotoxicity
  • nephrotoxicity
217
Q

AEs of fluoroquinololes

examples of fluoroquinolones

A
  • Gi intolerance, tendonitis, tendon rupture
  • ciproflaxin, levofloxacin, moxifloxacin
218
Q

anesthetic implcation of macrolides

A

CYP450 inhibition

219
Q

antibiotics that cause skeletal muscle weakness

A
  • aminoglycosides
  • clindamycin
220
Q

why is hypotension associated with vancomycin admin?

A

histamine release

221
Q

likelihood of cross reactivity between PCNs and cephalosporins

A

report of up to 10% overstated - true rate < 1%

222
Q

which cephalosporins are assoc, with lowest rate of cross reactivity with PCNs

A

3rd & 4th generation

223
Q

acceptable alternatives to cephalosporins with true PCN allergy

A
  • vancomycin
  • clindamycin
224
Q

most common side effect of prophylactic antibiotics

A

pseudomembranous colitis

225
Q

MOA of cephalosporins

A

disrupt bacterial cell wall synthesis (peptidoglycan)

226
Q

MOA of vancomycin

A

disrupts bacteral cell wall synthesis

227
Q

how often should cefazolin be redosed during surgery

228
Q

drug of choice for pts with active MRSA

A

vancomycin

229
Q

how to reduce histamine release and hypotension with vancomycin

A

admin at a rate of 10-15 mg/kg over 1 h

230
Q

how to minimize response to vancomycin

A

1 mg/kg diphenhdyramine + 4 mg/kg cimetidine 1 hr before anesthesia

231
Q

antibiotics contraindicated in pregnancy

A
  • chloramphenicol
  • erythromycin
  • fluoroquinolones
  • tetracyclines
232
Q

preferred method of skin prep before CVL placement according to the CDC

A

chlorohexidine

233
Q

consideration for use of alcohol based products for surgical prep

A

flammable, allow to dry for 2 minutes

234
Q

SCIP protocol

A
  • prophylactic antibiotic admin within 60 min of incision (vanc is 120 min)
  • antibiotic choice det. by surgery site
  • prophylactic abx d/c’d within 24 hours postop (48 hrs for heart pts)
  • glycemic control required for cardiac surgery (<200 mg/dL)
  • postop wound infection dx during initial hospitalization
  • surgical pts receive appropriate hair removal
  • colorectal pts normothermic upon arrival to PACU ( > 36 C)
235
Q

seroconversion rates after exposure to HIV-infected blood

A
  • needle stick = 0.3%
  • mucous membrane exposure = 0.09%
236
Q

what is Creutzfeldt-Jakob disease

3 etiologies

A

prion disease that can lead to encephalopathy and dementia

  1. consuming contaminated animal protein
  2. contaminated implants (corneal or dural tissue)
  3. cadaveric pituitary hormone supplementation
237
Q

precautions for Creutzfeld-Jakob disease

238
Q

main target of mycobacterium tuberculosis

A

anterior apical lung segments

239
Q

s/s tuberculosis

A
  • productive cough
  • hemoptysis
  • weight loss
  • fever
  • night sweats
  • anorexia
  • general malaise
240
Q

positive TB skin test result

A

site of induration > 10 mm (>5 mm if pt is immunocompromised)

241
Q

positive findings on CXR of TB pt

A

apical infiltrates and nodules

242
Q

if a skin TB test is positive but a CXR is negative, is TB ruled out?

243
Q

first line agent for TB treatment
what are its side effects?

A
  • isoniazid
  • peripheral neuropathy, hepatotoxicity
244
Q

what med can be added with isoniazid to reduce incidence of liver damage

A

pyridoxine

245
Q

adverse effects of rifampin

A
  • thrombocytopenia
  • leukopenia
  • anemia
  • kidney failure
  • orange urine/sweat/tears
246
Q

procedure with the highest risk of skin test conversion in healthcare personnel

2nd highest?

A

bronchoscopy

2 - intubation

247
Q

safety measures for pts with TB

A
  • providers and staff wear N95
  • HEPA filter placed between y-piece and airway
  • bacterial filter on expiratory limb of circuit
  • dedicated anesthesia machine and ventilator ideal
  • pre and postop care in negative pressure isolation room
248
Q

how long should elective procedures be delayed in pts with TB?

A
  • pt on antituberculosis chemo
  • 3 negative acid-fast bacillus tests
  • demonstrates symptom improvement
249
Q

most abundant WBC
what is its purpose

A

neutrophils

immune defense (bacterial and fungal)

250
Q

granulocyte that is an essential component of allergic reactions

251
Q

what is released by basophils in an allergic reaction

A
  • leukotrienes
  • histamine
  • prostaglandins
252
Q

how does epinephrine help in an allergic reaction?

A

prevents degranulation (release of intracellular contents) by binding to beta 2 receptors on cell membrane

253
Q

granulocytes that defend against parasites

A

eosinophils

254
Q

purpose of monocytes

A

fight bacterial, viral, and fungal infection (phagocytosis)

255
Q

function of B-lymphocytes

A

humoral immunity (produce antibodies)

256
Q

function of T-lymphocytes

A

cell-mediated immunity (does not produce antibodies)

257
Q

function of natural killer cells
meds that reduce their function

A

limit spread of tumor and microbial cells

opioids reduce function (concern of cancer recurrence)

258
Q

which agranulocyte releases cytokines

259
Q

anaphylaxis is an example of which type of hypersensitivity reaction?

260
Q

ABO incompatibility is an example of which type of hypersensitivity reaction?

261
Q

serum sickness after a snake bite is an example of which type of hypersensitivity reaction?

262
Q

graft vs host reaction is an example of which type of hypersensitivity reaction?

263
Q

what is the difference in an anaphylactic and an anaphylactoid reaction?

A

anaphylaxis requires prior sensitization or cross-reactivity

no prior exposure needed for anaphylactoid reactions

264
Q

effects of H1 receptor activation

A
  • vasodilation
  • increased vascular permeability
  • smooth muscle contraction (not vascular)
265
Q

effects of H2 receptor activation

A
  • tachycardia
  • gastric acid secretion
266
Q

metabolites of arachidonic acid

what are the effects of release

A
  • leukotrienes
  • prostaglandins

bronchoconstriction and vasodilation

267
Q

CV effects of hypersensitivity reactions

A
  • hypotension
  • tachycardia
  • arrythmia
  • cardiac arrest
268
Q

respiratory symptoms of hypersensitivity reaction

A
  • bronchospasm
    decreased ETCO2
    decreased SaO2
    increased PIP
  • laryngeal edema
  • increased mucous production
269
Q

GI effects of hypersensitivity reactions

A
  • abdominal cramping
  • N/V/D
270
Q

what causes a type 1 hypersensitivity reaction

A

antigen + antibody interaction in a patient who has previously been sensitized to the agent

271
Q

which hypersensitivity reaction is IgE-mediated

272
Q

which hypersensitivity reaction is an immediate reaction

273
Q

extrinsic asthma is an example of what type of hypersensitivity reaction

274
Q

what is the best lab test to determine if an allergic response has occured?

A

tryptase (released from mast cells during an allergic reaction)

275
Q

which type of hypersensitivity reaction is antibody-mediated

276
Q

antibodies involved in type 2 hypersensitivity reaction

277
Q

what causes a type 3 hypersensitivity reaction

A

immune complex is formed and deposited into the patient’s tissue (normally cleared from body)

278
Q

which types of hypersensitivity reactions activate the complement cascade

A

type 2 & 3

279
Q

how long is an allergic reaction delayed in a type 4 hypersensitivity reaction

A

at least 12 hours after exposure

280
Q

dose of epi for intraoperative anaphylaxis

A

5-10 mcg IV for hypotension
0.1-1 mg IV for CV collapse

281
Q

histamine antagonists that should be given during intraoperative anaphylaxis

A
  • H1 blocker: diphenhydramine 0.5-1 mg/kg
  • H2 blocker: ranitidine 50 mg Iv or famotidine 20 mg IV
282
Q

dose and use of hydrocortisone in intraoperative anaphyalxis

A

250 mg IV - prevents delayed release of inflammatory compounds (no immediate effect)

283
Q

med to use for refractory hypotension in intraoperative anaphylaxis

A

vasopressin - start at 0.01 unit/min

284
Q

3 ways epinephrine treats anaphylaxis

A
  1. prevents degranulation
  2. CV support
  3. airway dilation
285
Q

top 3 most common causes of perioperative anaphylaxis

A
  1. NMBs (succs most common)
  2. latex
  3. antibiotics (beta lactams most common)
286
Q

groups at high risk for latex reaction

A
  • spina bifida/myelomeningocele
  • atopy
  • health care workers
  • allergy to banana, kiwi, mango, papaya, pineapple, tomato
287
Q

side effects of cisplatin

A

acoustic nerve injury
nephrotoxicity

288
Q

side effects of vincristine and vinblastine

A

peripheral neuropathy

289
Q

side effects and anesthesia implications of bleomycin

A

pulmonary fibrosis
keep FiO2 < 30%

290
Q

main adverse effect of doxorubicin

A

cardiotoxicity

291
Q

most chemotherapeutic agents cause bone marrow suppression and thrombocytopenia. which is a key exception?

292
Q

5 key hormones that regulate digestive activity

A
  1. gastrin
  2. secretin
  3. cholecystokinin
  4. gastric inhibitory peptide
  5. somatostatin
293
Q

function of gastrin

where is it produced

A
  • increased gastric acid secretion when food enters stomach
  • increased pepsinogen secretion (converts to pepsin and aids in protein digestion)

produced in G cells of stomach

294
Q

function of secretin

where is it produced

A
  • pancreatic bicarbonate secretion
  • decreased gastrin secretion
  • liver secretes bile

produced in S cells of small intestine

295
Q

function of cholecystokinin

where is it produced

A
  • gallbladder contraction
  • increased pancreatic enzyme secretion

produced in I cells of small intestine

296
Q

function of gastric inhibitory peptide

where is it produced

A
  • increased insulin reelase
  • slows gastric emptying
  • decreased gastric motility

K cells of small intestine

297
Q

hormone that is the universal “off” switch for digestion (decreases all GI function)

A

somatostatin

298
Q

where is somatostatin produced

A

D cells in pancreatic islet, stomach, small intestine

299
Q

digestive hormone increased in Zolliger-Ellison syndrome

300
Q

digestive enzyme that causes gallbladder pain after a fatty meal

A

cholecystokinin

301
Q

digestive enzyme that is the treatment for carcinoid tumors

A

somatostatin

302
Q

what determines the likelihood of gastroesophageal reflux

A

barrier pressure
increased barrier pressure = decreased likelihood of reflux

303
Q

3 things that reduce gastric barrier pressure

A
  • anticholinergics (dec. LES tone)
  • cricoid pressure ( dec. LES tone)
  • pregnancy (dec. LES tone and inc. intragastric pressure)
304
Q

what drug increases gastric barrier pressure

A

metoclopramide (inc. LES tone)

305
Q

does succs affect gastric barrier pressure?

A

no - increased LES tone + increased intragastric pressure = 0 net change

306
Q

gastric barrier pressure =

A

LES pressure - intragastric pressure

307
Q

where does ondansetron antagonize serotonin receptors?

A
  1. chemoreceptor trigger zone
  2. peripheral receptors in GI tract and vagus nerve
308
Q

where is the vomiting center located

A

nucleus tractus solitarus (medulla)

309
Q

where does sensory input to the vomiting center arise from?

A

chemoreceptor trigger zone, GI tract, and vestibular system

310
Q

receptors in the CTZ

A
  • serotonin (5HT3)
  • substance P (NK-1)
  • dopamine
  • opioid
311
Q

5-HT3 antagonists used as antiemetics & their normal doses

A
  • ondansetron: 4-8 mg
  • granisetron: 1 mg
  • dolasetron: 12.5 mg
312
Q

NK-1 antagonist used as an antiemetic

A

aprepitant

313
Q

dopamine antagonists used as antiemetics & normal doses

A
  • metoclopramide: 10-20 mg
  • droperidol: 0.625-1.25 mg
  • haloperidol: 0.5-2 mg
  • midazolam (may antagonize dopamine receptors in CTZ)
314
Q

receptors associated with the vestibular apparatus

what drugs antagonize these receptors?

A

histamine (H1) - diphenhydramine
acetylcholine - scopolamine

315
Q

opioid receptors reside in what sensory inputs to the vomiting center

A

vestibular apparatus
CTZ

316
Q

how does the GI tract stimulate the vomiting center?

317
Q

antiemetics that target the GI tract

A

5-HT3 antagonists
NK-1 antagonist (Aprepitant)

318
Q

normal Aprepitant dose

319
Q

patient risk factors for PONV

A
  • female
  • nonsmoker
  • history of motion sickness
  • previous PONV
  • younger age (loose association)
320
Q

surgical risk factors for PONV

A
  • long duration (>1 hour)
  • GYN procedures
  • laparoscopy
  • breast
  • plastics
  • peds: strabismus, orchiopexy, T&A
321
Q

anesthetic risk factors for PONV

A
  • halogenated anesthetics
  • N2O > 50%
  • opioids
  • etomidate
  • neostigmine
322
Q

what explains why the CTZ is stimulated by noxious chemicals

A

BBB poorly developed at CTZ

323
Q

most common SEs of ondansetron

A
  • HA
  • diarrhea
324
Q

when should decadron be given for PONV prophylaxis?

A

during induction

325
Q

antiemetics that are contraindicated in pts with Parkinson’s

A

dopamine antagonists (phenothiazines, metoclopramide) - can cause extrapyramidal symptoms

326
Q

antiemetic contraindicated in bowel obstruction

A

metoclopramide (d/t prokinetic effect)

327
Q

what causes motion-induced nausea

A

M1 & H1 stimulation in vestibular system of inner ear

328
Q

what type of antiemetic should pts undergoing middle ear surgery receive?

A

agents that target vestibular system

329
Q

best time to apply scopolamine?

how long does it last

A

> 4 hours before anesthesia induction

lasts for 72 hours

330
Q

dose of propofol that produces an antiemetic effect

331
Q

how can midazolam reduce PONV?

A

decreasing dopamine activity in CTZ

332
Q

how does ephedrine affect PONV?

A

25 mg IM may reduce by maintaining BP and cerebral perfusion

333
Q

significance of P6 acupressure point

A

nonpharmacologic method of reducing PONV - located 3 fingerbreadths below wrist on inner forearm in between 2 tendons

334
Q

when should ondansetron be admin for PONV prophylaxis?

A

30 min before emergence

335
Q

best class of antiemetics for patients undergoing mastoidectomy

A

anticholinergics

336
Q

transient physiologic changes after release of pneumatic tourniquet

A
  • increased ETCO2
  • increased core body temp
  • decreased BP
  • decreased SvO2 (SaO2 usually normal)
  • metabolic acidosis
337
Q

symptoms of bone cement implantation syndrome

A
  • V/Q mismatch (increased dead space)
  • right heart failure in extreme cases
  • bradycardia
  • dysrhythmias
  • hypotension (dec. SVR)
  • pHTN (inc. PVR)
  • hypoxia
  • cardiac arrest
338
Q

surgery assoc. with highest risk of BCIS
other surgeries with high risk

A

hip arthroplasty

knee arthroplasty, vertebroplasty, kyphoplasty

339
Q

first signs of BCIS in awake patient under regional anesthesia

A
  • dyspnea
  • AMS
340
Q

first sign of BCIS in anesthetized pt

A

decreased ETCO2

341
Q

first line treatment of BCIS

A
  • 100% FiO2
  • IV hydration
  • phenylephrine for hypotension
342
Q

when is fat embolization syndrome risk greatest?

A

within first 72 hours of long bone injury

343
Q

risk factors for fat embolization syndrome

A
  • pelvic fracture
  • femoral fracture
  • instrumentation of femoral medullary canal
344
Q

triad of fat embolization syndrome

A
  • respiratory insufficiency (hypoxemia, bil. CXR infiltrates, ARDS)
  • neuro involvement (confusion to coma)
  • petechial rash (neck, axilla, oral mucosa, conjunctiva)
345
Q

treatment of fat embolization syndrome

A

supportive; corticosteroids may or may not improve outcomes (controversial)

346
Q

pneumatic tourniquet inflation pressure for upper extremity surgery

A

70-90 mmHg above SBP

347
Q

pneumatic tourniquet inflation pressure for lower extremity surgery

A

2x over SBP

348
Q

why does the tourniquet for a bier block have to be inflated for at least 20 min

A

premature release increases risk of seizure/cardiac arrest with LAST

349
Q

tourniquet inflation pressure for upper extremity bier block

A

250 mmHg or 100 mmHg over SBP (whichever is higher)

350
Q

tourniquet inflation pressure for lower extremity bier block

A

350-400 mmHg

351
Q

what is Samter’s triad and what are the 3 components

A

aspirin-exacerbated respiratory disease - can develop life threatening bronchospasm after aspirin admin

  • asthma
  • allergic rhinitis
  • nasal polyps
352
Q

effects of COX-1 inhibition

A
  • impaired platelet function
  • gastric irritation
  • reduced renal blood flow
353
Q

which COX enzyme is expressed during inflammation

354
Q

effects of COX-2 inhibition

A
  • analgesia (ceiling effect)
  • anti-inflammatory effects
  • antipyretic effects
355
Q

CV complications of NSAIDs

A

increased risk of HTN, MI, HF (COX-2 inhibitors > COX-1)

356
Q

pulmonary complication of NSAIDs

A

dec. prostaglandins = leukotrienes = bronchospasm

357
Q

hematologic complication of NSAIDs

A

platelet inhibition = increased bleeding risk

358
Q

renal complication of NSAIDs

A

decreased prostaglandins = decreased renal blood flow (avoid in renal disease)

359
Q

CNS complication of NSAIDs

360
Q

bone related complication of NSAIDs

A

decreased osteoclast and osteoblast activity may impair bone healing

361
Q

GI complications of NSAIDs

A

gastric ulceration and bleeding

362
Q

NSAID drug interactions

A

NSAIDs displace albumin bound drugs and increase their plasma concentration (warfarin, phenytoin, valproic acid)

363
Q

why have most COX-2 inhibitors been removed from the market

A

concerns about CV risk

364
Q

max amount of time ketorolac can be taken

365
Q

___ mg ketorolac = 10 mg morphine

366
Q

MOA of aspirin

A

irreversibily inhibits COX-1 and COX-2
platelet inhibition lasts for the life of the platelet

367
Q

suggested MOA of acetaminophen

A

inhibits prostaglandin synthesis (COX-3 inhibition?)

analgesia may be from activation of descending inhibitory pain pathway in spinal cord

368
Q

acid base imbalance seen with aspirin toxicity

A

gap metabolic acidosis

369
Q

max daily dose of tylenol

370
Q

6 drugs that inhibit the COX-2 pathway

A
  1. aspirin
  2. ibuprofen
  3. naproxen
  4. ketorolac
  5. diclofenac
  6. indomethacin
371
Q

perioperative implication of licorice as an herbal supplement

A

may mimic Conn’s syndrome:
- mimics effects of aldosterone
- sodium and water retention with decreased K+

372
Q

perioperative implications of valerian root as an herbal medication

A
  • decreases MAC (increased GABA)
  • may prolong duration of anesthetics
  • abrupt discontinuation can cause withdrawal
373
Q

perioperative implication of St. Jon’s Wort as an herbal medication

when should it be d/c’d before surgery?

A
  • serotonin syndrome with MAOIs
  • CYP3A4 induction
  • decreased serum level of warfarin, protease inhibitors, digoxin
  • may prolong anesthetic agent duration

d/c 5 days preop

374
Q

perioperative implication of garlic as an herbal medication

when should it be d/c’d before surgery?

A
  • increased bleeding risk
  • decreased serum glucose

d/c 7 days preop

375
Q

ephedra (Ma Huang) interactions and toxicity

A
  • serotonin syndrome with MAOIs
  • catecholamine depletion with long term use (HD instability)
  • sympathomimetic effects
376
Q

anesthetic implications of ginger as an herbal supplement

A

increased bleeding risk

377
Q

anesthesia implications of ginseng as an herbal supplement

A
  • increased bleeding risk
  • enhanced SNS effects of sympathomimetics
  • may cause hypoglycemia (risk in fasting patient)
378
Q

anesthesia implicaitons of kava kava as an herbal supplement

A
  • decreased MAC (increased GABA)
  • may prolong duration of anesthetic agents
379
Q

anesthetic implications of Saw Palmetto

A

increased bleeding risk

380
Q

4 herbal supplements that increase the risk of bleeding

A
  • Garlic
  • Ginger
  • Gingko
  • Ginseng

(4 G’s)

381
Q

ASA Pre-Anesthesia Checkout Procedure recommendations - tasks to complete before every patient

A
  • verify suction
  • check function of monitors and alarms
  • check vaporizers filled, ports closed
  • check CO2 absorbent
  • high pressure leak test
  • assess unidirectional valves
  • document
382
Q

what agency sets the standards for required components of the anesthesia machine

A

american society for testing and materials

383
Q

agency that sets the standards for compressed gas cylinders

A

US department of transportation

384
Q

agency that sets the standards for food and drugs

385
Q

agency that created the 1993 Anesthesia Machine Pre-Use Checkout procedures

386
Q

agency that sets standards for acceptable occupational exposure to volatiles

387
Q

agency that certifies hospitals that meet specific safety standards

A

Joint Commission (JCAHCO)

388
Q

MRI zone 1

A

public access, requires no supercision

ex- hallway outside MRI Suite

389
Q

MRI zone 2

A

public access + minimal supervision

ex- entrance to MRI suite

390
Q

MRI safety zone 3

A

limited access + strict supervision

ex- MRI control room

391
Q

MRI zone 4

A

very limited access + very strict supervision

ex- MRI scanner room

392
Q

T/F - ferromagnetic objects are allowed in MRI zone 4

393
Q

safe metals in MRI suite

A

stainless steel
titanium
aluminum
copper

394
Q

common side effect of IV contrast media

395
Q

EKG changes that may be seen in MRI

A

T wave and ST segment artifacts

396
Q

what indicates an MRI safe gas cylinder

A

silver with a color code at the top

397
Q

estimated anesthetic mortality assoc. with each ASA class

A

1 - 0.04 per 10,000 anesthetics
2 - 0.5 per 10,000
3 - 2.7 per 10,000
4 - 5.5 per 10,000

398
Q

according to closed claims analysis, what are the 4 most common causes of injury (in order) that result in claims filed?

A
  1. regional anesthesia (20%)
  2. respiratory events (17%)
  3. CV events (13%)
  4. equipment failure (10%)
399
Q

what is the modified Aldrete scoring system

A

used to quantify readiness for discharge from PACU

assesses 5 things:
activiy, respiration, circulation, consciousness, O2 sat

400
Q

modified Aldrete score that suggests readiness for PACU discharge

A

score of 9 or greater

401
Q

modified Aldrete scoring system: Activity

A

2: moves all extremities voluntarily or on command and can lift head
1: moves 2 extremities voluntarily or on command and can lift head
0: cannot move extremities or lift head

402
Q

modified Aldrete scoring system: Respirations

A

2: breathes normally, can cough effectively
1: dyspneic, shallow, or otherwise inadequate breathing
0: apneic

403
Q

modified Aldrete scoring system: Circulation

A

2: BP within 20 mmHg of preanesthetic value (min SBP = 90)
1: BP within 20-50 mmHg of preanesthetic value
0: BP > 50 mmHg of preanesthetic value

404
Q

modified Aldrete scoring system: Consciousness

A

2: fully awake
1: arousable to voice
0: unresponsive to voice but may be responsive to painful stimuli

405
Q

modified Aldrete scoring system: O2 sat

A

2: SpO2 > 92% on RA
1: SpO2 > 90% but needs supplemental O2
0: SpO2 < 90% on supplemental O2

406
Q

time to onset of sympathomimetic syndrome

A

up to 30 min

407
Q

causes of sympathomimetic syndrome

A

amphetamines

cocaine

408
Q

key features of sympathomimetic syndrome

A
  • agitation
  • hallucinations
  • arrhythmias
  • myocardial ischemia
409
Q

treatment of symapthomimetic syndrome

A

vasodilators

labetolol

410
Q

time to onset of TCA overdose

A

up to 6 hours

411
Q

key features of TCA overdose

A
  • hypotension
  • dec. LOC/coma
  • polymorphic VT
412
Q

treatment of TCA overdose

A

magnesium

serum alkalization

413
Q

time to onset of serotonin syndrome

A

up to 12 hours

414
Q

drugs that can cause serotonin syndrome

A
  • SSRIs
  • SNRIs
  • MAOIs
  • ecstasy
415
Q

key features of serotonin syndrome

A
  • akathisia
  • mydriasis
  • tremor
  • AMS
  • clonus
  • muscle rigidity
416
Q

treatment of serotonin syndrome

A

cyproheptadine (5-HT2A blocker)

417
Q

time to onset of anticholinergic syndrome

A

up to 12 hours

418
Q

causes of anticholinergic syndrome

A

atropine

scopolamine

419
Q

key features of anticholinergic syndrome

A
  • red, hot, dry skin
  • mydriasis
  • delirium
420
Q

time to onset of NMS

A

up to 24-72 hours

421
Q

key features of NMS

A
  • bradykinesia
  • dec. LOC/coma
  • rhabdo
  • myoglobinuria
  • acidosis
  • ANS instability
  • muscle rigidity
  • normal pupils
422
Q

treatment of NMS

A

bromocriptine

dantrolene

ECT

APEX (54 decks)

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